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About Me

Hi! My name is Qadoshyah and I'm the oldest of 11 kids. I live on a ranch in the beautiful country of Northeastern Oklahoma with my family. We are a large household with so many kids that we have various projects going on: We raise goats, pigs, sheep, and rabbits (I raise the rabbits - cute little mini lops) on our 44 acre ranch. Our ranch is also home to bullmastiffs, chickens, guinea hens, ducks, llamas, a donkey, a bottle calf, and several ranch dogs and livestock guardian dogs. The youngest two kids are boy/girl twins born in Feb. '05. The boy happens to have Down syndrome. He is such a blessing to our family :)! Our whole family is also gluten-free, which adds another interesting aspect to our large, active family. We also cook dairy-free & corn-free due to allergies a few kids have. Some of the family is also on the GAPS diet to restore gut health.

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The writers of this blog research and attempt to give what they believe is the most accurate and up-to-date information. Nonetheless, the information on this blog is simply opinions and does not in any way constitute professional legal or medical advice. Also, references or links to external, or third party websites, are provided solely for visitors' convenience and are not controlled nor monitered by us. Links taken to other sites are done so at your own risk.

Moreover, this blog and it's writers do not endorse or support religious views that are not consistent with the Bible. The only faith we have found that is faithful to Scripture can be found at www.atruechurch.info.

Down Syndrome (DS) is a genetic disorder that affects ~1 in 700 live births, caused by trisomy of human chromosome 21 (Hsa21), and results in cognitive impairment, craniofacial abnormalities, low muscle tone, and skeletal deficiencies. To study these phenotypes, we utilized the Ts65Dn mouse model, which contains three copies of approximately half the orthologous found on Hsa21 and exhibits similar phenotypes as found in humans with DS. Individuals with DS and Ts65Dn mice have deficits in bone mineral density (BMD), architecture, and bone strength. Over-expression of DYRK1A, a serine-threonine kinase encoded on Hsa21, has been linked to deficiencies in DS bone homeostasis. Epigallocatechin-3- gallate (EGCG), an aromatic polyphenol found in high concentrations in green tea, is a known inhibitor of Dyrk1a activity. Normalization of Dyrk1a activity by EGCG may have the potential to regulate bone homeostasis and increase BMD and bone strength in individuals with DS. In this study, we hypothesized that EGCG obtained from different sources would have differential effects in correcting bone deficits associated with DS. To test our hypothesis, we performed on EGCG and related compounds from different sources. The LC-MS analysis determined the amount of EGCG and the degradation in our stock solution. Next, we treated three-week- old Ts65Dn and control male mice with EGCG for three weeks. At six weeks of age, mice were sacrificed. DXA and micro CT analysis were performed on the femurs and skulls of the mice to assess trabecular and cortical bone structure and BMD. Our results indicate the ability of EGCG to ameliorate skeletal deficiencies and compared pure EGCG with EGCG purchased from commercial vendors in correcting skeletal deficits associated with DS.